Acquisition of CD40 Expression During Murine B‐Cell Differentiation

Grandien, Alf; Bras, Alexandra Le; Martı́nez-A, Carlos

doi:10.1046/j.1365-3083.1996.d01-13.x

Cited by 4 publications

(3 citation statements)

References 24 publications

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“…All of these receptors are expressed in developing B cells and pre- and immature mouse B cell lines27,28, and all activate NF-κB and induce transcription of genes encoding pro-survival proteins. We therefore examined the proportions of Igλ + cells in the immature B cell compartments of mice lacking Bcl10 and MyD88, which mediate NF-κB activation downstream of these receptors1,29, or CD40.…”

Section: Resultsmentioning

confidence: 99%

Development of immunoglobulin λ-chain–positive B cells, but not editing of immunoglobulin κ-chain, depends on NF-κB signals

et al. 2009

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By genetically ablating IκB kinase (IKK)-mediated NF-κB activation in the B cell lineage, and by analyzing a mouse mutant in which Igλ+ B cells are generated in the absence of rearrangements in Igk, we define two distinct, consecutive phases of early B cell development that differ in their dependence on IKK-mediated NF-κB signaling. During the first phase, in which NF-κB signaling is dispensable, predominantly Igκ+ B cells are generated and undergo efficient receptor editing. In the second phase, predominantly Igλ+ B cells are generated, whose development is ontogenetically timed to occur after Igk rearrangements. This second phase of development is dependent on NF-κB signals, which can be substituted by transgenic expression of the pro-survival factor Bcl2.

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Section: Resultsmentioning

confidence: 99%

Development of immunoglobulin λ-chain–positive B cells, but not editing of immunoglobulin κ-chain, depends on NF-κB signals

et al. 2009

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“…To determine whether CD2:Stat6VT B cells are activated or simply have increased expression of Stat6-inducible genes, we analyzed the expression of other cell surface markers that indicate activation or maturation of B lymphocytes and are not regulated by IL-4. FACS analysis of freshly isolated B220 ϩ cells from wildtype and CD2:Stat6VT mice showed that CD40 expression, which is up-regulated on activated or mature B lymphocytes (43)(44)(45), was increased on transgenic B cells compared with wild type (Fig. 5A).…”

Section: Stat6vt Does Not Induce An Activated Phenotype In B Lymphocytesmentioning

confidence: 99%

Expression of a Constitutively Active Stat6 In Vivo Alters Lymphocyte Homeostasis with Distinct Effects in T and B Cells

Bruns

Schindler²,

Kaplan

2003

The Journal of Immunology

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IL-4 is a critical cytokine in the regulation of immune responses and genesis of atopy. Engagement of the IL-4R activates multiple signaling pathways, including the transcription factor Stat6. Stat6-deficient mice demonstrate the importance of this factor in lymphocyte proliferation, gene expression, and Th cell differentiation. Recently, a mutant Stat6 (Stat6VT) was generated that is transcriptionally active independent of IL-4 stimulation. To determine the ability of a constitutively active Stat6 to mimic IL-4-stimulated responses, we have generated transgenic mice expressing Stat6VT under control of the CD2 locus control region, restricting expression to lymphoid populations. The phenotype of Stat6VT transgenic mice is similar, but not identical, to IL-4 transgenic mice, suggesting a critical role for Stat6-independent signaling pathways in the generation of some IL-4 responses in vivo. The expression of a constitutively active Stat6 in vivo increases surface expression of IL-4-induced genes and increases serum levels of IgG1 and IgE, compared with nontransgenic mice. Stat6VT expression increases Th2 differentiation in vivo and in vitro. Stat6VT expression also dramatically alters homeostasis of peripheral lymphocyte populations resulting in decreased CD3+ cells and increased B220+ cells, compared with nontransgenic littermates. Altered T and B cell populations correlate with an activated phenotype and increased cell death in transgenic T cell, but not B cell, populations. Together these results suggest that expression of a constitutively active Stat6 has distinct effects on B and T lymphocytes.

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“…The low basal expression of CD40, together with its induced expression in inflammation, suggest that CD40 ligation is particularly relevant in inflammatory conditions; its increased expression by inflammatory mediators provides a mechanism for amplification in inflammation. The induction of CD40 expression upon podocyte differentiation may suggest that, as for other cell types [Castigli et al, 1996;Grandien et al, 1996;Ma and Clark, 2009], CD40 expression is a feature of cell maturation. How CD40 signaling regulates ECM homeostasis has been for a large part studied in the vascular system, but its role in other tissue remains ill understood.…”

mentioning

confidence: 99%

CD154 Induces Matrix Metalloproteinase‐9 Secretion in Human Podocytes

Rigothier

Daculsi

Lepreux

et al. 2016

J of Cellular Biochemistry

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Matrix remodeling is a key feature of glomerulosclerosis secondary to diabetes or hypertension. Podocytes contribute to glomerular basement membrane (GBM) turnover by producing matrix components and matrix remodelling enzymes, including matrix metalloproteinases (MMPs). The CD40/CD154 signaling pathway modulates matrix remodeling through the synthesis of MMPs and tissue inhibitors of MMPs. Platelets are a primary blood reservoir of CD154. Here we studied, the impact of the CD154/CD40 pathway on MMP-9 expression by cultured human podocytes. The role of CD40/CD154 was evaluated upon exposure of podocytes to recombinant human CD154 (rhCD154) or activated platelet supernatants from healthy human subjects. We first showed by protein and mRNA expression that CD40 was synthesized by podocytes and detectable on kidney tissue sections. CD40 expression was acquired during podocyte differentiation and enhanced upon exposure to rhCD154. In podocytes, rhCD154 induced an increase of MMP-9 production as shown by RT-PCR, Western blot and and gelatin zymography. Activated platelet supernatants induced MMP-9 mRNA synthesis in podocytes, an effect reduced by anti-CD40 antibody. Our results underscore a potential role for platelets through the CD40/CD154 signaling pathway in the control of GBM synthesis and degradation, via its regulatory role on MMP-9 production. CD154 secretion by activated platelets may contribute to GBM alterations in proteinuric nephropathies. J. Cell. Biochem. 117: 2737-2747, 2016. © 2016 Wiley Periodicals, Inc.

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Acquisition of CD40 Expression During Murine B‐Cell Differentiation

Cited by 4 publications

References 24 publications

Development of immunoglobulin λ-chain–positive B cells, but not editing of immunoglobulin κ-chain, depends on NF-κB signals

Development of immunoglobulin λ-chain–positive B cells, but not editing of immunoglobulin κ-chain, depends on NF-κB signals

Expression of a Constitutively Active Stat6 In Vivo Alters Lymphocyte Homeostasis with Distinct Effects in T and B Cells

CD154 Induces Matrix Metalloproteinase‐9 Secretion in Human Podocytes

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